共 67 条
APP processing and synaptic function
被引:1321
作者:

Kamenetz, F
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机构: Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA

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Hsieh, H
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机构: Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA

Seabrook, G
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h-index: 0
机构: Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA

Borchelt, D
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机构: Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA

Iwatsubo, T
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h-index: 0
机构: Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA

Sisodia, S
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h-index: 0
机构: Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA

Malinow, R
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机构: Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA
机构:
[1] Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA
[2] SUNY Stony Brook, Grad Program Genet, Stony Brook, NY 11794 USA
[3] SUNY Stony Brook, Grad Program Neurosci, Stony Brook, NY 11794 USA
[4] Univ Tokyo, Grad Sch Pharmaceut Sci, Dept Neuropathol & Neurosci, Tokyo, Japan
[5] Merck & Co Inc, Merck Res Labs, West Point, PA 19486 USA
[6] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21287 USA
[7] Univ Chicago, Ctr Mol Neurobiol, Dept Neurobiol Pharmacol & Physiol, Chicago, IL 60637 USA
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关键词:
D O I:
10.1016/S0896-6273(03)00124-7
中图分类号:
Q189 [神经科学];
学科分类号:
071006 ;
摘要:
A large body of evidence has implicated Abeta peptides and other derivatives of the amyloid precursor protein (APP) as central to the pathogenesis of Alzheimer's disease (AD). However, the functional relationship of APP and its proteolytic derivatives to neuronal electrophysiology is not known. Here, we show that neuronal activity modulates the formation and secretion of Abeta peptides in hippocampal slice neurons that overexpress APP. In turn, Abeta selectively depresses excitatory synaptic transmission onto neurons that overexpress APP, as well as nearby neurons that do not. This depression depends on NMDA-R activity and can be reversed by blockade of neuronal activity. Synaptic depression from excessive Abeta could contribute to cognitive decline during early AD. In addition, we propose that activity-dependent modulation of endogenous Abeta production may normally participate in a negative feedback that could keep neuronal hyperactivity in check. Disruption of this feedback system could contribute to disease progression in AD.
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页码:925 / 937
页数:13
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